Abstract
Macropinocytosis is a type of large-scale endocytosis that is triggered by the interaction of receptor proteins and ligands, such as growth factors, cytokines, chemokines, and lipopolysaccharide (LPS). Macropinocytosis ingests the extracellular fluid solutes and conveys them into the lysosome in the context of cell growth and differentiation. Aside from its physiological functions, macropinocytosis has been observed in viral infections. While the infectious mechanism of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is still unknown, recent studies suggest the involvement of macropinocytosis in its cell entry. In this review, we discuss the roles of endocytosis in SARS-CoV/SARS-CoV-2 cell entries and propose a hypothetical role of macropinocytosis in SARS-CoV-2 cell entry.
Highlights
Cell membrane dynamics are controlled precisely by signal transduction and cytoskeletal mechanisms[1−3]
We describe the molecular mechanism of SARS-CoV-2 cell entry, focusing on macropinocytosis
The African green monkey kidney cell line Vero E6 has been used as the standard model to investigate the molecular mechanism of cell entry because Angiotensin converting enzyme 2 (ACE2) was identified as the CoV-S target protein using Vero E6 lysates[63] and its expression level is robust[73]
Summary
Cell membrane dynamics are controlled precisely by signal transduction and cytoskeletal mechanisms[1−3]. Endocytosis is a cellular mechanism by which cells ingest extracellular components by modulating the plasma membrane. Based on their functions and mechanisms, endocytosis can be categorized into at least four different types[4−6]: clathrin-mediated endocytosis, caveolae-dependent. The pathogenic bacteria Salmonella typhimurium (2.0 –5.0 mm in length and 0.5 –1.5 mm in diameter) and Shigella flexneri (1.0–3.0 mm in length and 0.4–0.6 mm in diameter) inject their own proteins into the host cells to induce macropinocytosis as a means of cell entry[7,12−13]. The molecular function is not yet clear, the involvement of macropinocytosis in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) cell entry has been suggested[16]. We present an overview of studies on endocytosis and SARS-CoV cell entry as the background information. We describe the molecular mechanism of SARS-CoV-2 cell entry, focusing on macropinocytosis
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